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Printed with permission from Dr. Mark Stengler's Health Revelations (www.healthrevelations.com) By now, you are probably aware that there has been a lot of deception and misinformation out there about the link between cholesterol and heart disease. For decades, the mainstream medical community has led people to believe that elevated cholesterol is the culprit of heart disease. Mainstream doctors (and media) have told you to cut back on saturated fat, which science has shown to NOT reduce heart disease risk. You’re supposed to avoid foods high in cholesterol, such as eggs—also proven to be false, since most cholesterol in the body is manufactured by the liver and DOESN’T come from diet. And you’ve been practically forced to drive down your cholesterol levels as low as you can with prescription drugs that come with a laundry list of serious side effects. It turns out that most of propaganda is a bunch of baloney. Unfortunately, it will probably be another ten years before it becomes obsolete. If your doctor is still evaluating your cardiovascular risk purely based on an antiquated lipid panel that includes total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides, you should be concerned. Instead, you should stay ahead of the curve with meaningful cardiovascular screening tests that identify problems well in advance. I’ve been guiding my Health Revelations readers and patients with a much more sophisticated and effective way to identify your risk of heart disease… and to treat it once you’ve got it. You need to get a much better assessment so you can prevent against heart attack and stroke—and that includes looking for markers of inflammation that fuel the flames of artery damage and resulting plaque formation.
Fortunately, an increasing number of cardiologists have joined me in challenging the current theory of high cholesterol and heart disease. For example, cardiologist Dr. Stephen Sinatra proclaims (and rightly so) that the link between high levels of total cholesterol and heart disease is all theoretical and has NEVER been proven. His theory is that focusing on traditional cholesterol levels is a scam designed to stuff the coffers of drug companies who sell cholesterol-lowering drugs to the tune of billions of dollars annually.1This is a valid point, since it has been well known in conventional medicine that cholesterol levels are a poor predictor of heart attacks and heart disease. Case in point: Approximately 50 percent of people who have a heart attack do NOT have high cholesterol! Now, you may be thinking that it’s just total cholesterol that’s not a good marker of cardiovascular risk. After all, you’ve also been told that LDL cholesterol in particular is the villain when it comes to heart disease—and that you should worry if that number in particular is high. However, in a large study published in the American Heart Journal that analyzed the data of more than 230,000 people hospitalized with coronary artery disease, researchers found that about 50 percent of these people had LDL levels that were WAY under the “normal” number. While most labs would deem less than 130 mg/dL to be the goal (unless one has diabetes or existing heart disease the reference range is lower), half of these folks with heart disease bad enough to land them in the hospital showed LDL levels that were less than 100 mg/dL!2
Recently, a patient came to my office to show me the results of a cholesterol test ordered by her primary doctor. Her doctor had recommended that she start on a cholesterol-lowering statin drug because her total cholesterol was 203 mg/dL. I could not believe it! A normal range is less than 200 mg/dL, which means she was just BARELY over the threshold! But this just goes to show that some doctors practice like they are automated machines. They see a certain value on a test and automatically prescribe a drug. Heck, with medical practice standards like this, you might as well consult with a robot. Anyone so concerned about getting their total cholesterol down by just FOUR POINTS—or even more—could simply do it by exercising more or by increasing certain foods in their diet, such as oatmeal, almonds, walnuts, flaxseeds, and garlic. Why would one take a cholesterol-lowering drug to reduce their total cholesterol by four points when it increases their risk of diabetes (by almost 50 percent), memory problems, joint pain, muscle pain, fatigue, liver and kidney damage, and possibly even cancer? It’s craziness!
It’s pretty clear that we’ve been led by some bad science when it comes to determining risk for heart disease. In the words of Dr. Sinatra, “One of my top missions has been to educate people on the true cause of heart disease, and it’s not cholesterol. Most doctors and cardiologists are still testing their patients’ cholesterol numbers and wearing out their prescription pads with orders for prescription-lowering statin drugs. Meanwhile the true cause of heart disease, inflammation, is still largely ignored.”3 That’s right—most docs have been looking at the WRONG THING in assessing your risk, and they’ve been prescribing meds to lower a number that’s essentially MEANINGLESS when it comes to heart disease!Now, let’s look at some good science—particularly as it relates to one of the most important markers of inflammation. Known as Lipoprotein-associated phospholipase A2, abbreviated Lp-PLA2, this marker is an enzyme that accumulates in artery plaque. It’s thought to play an important role in plaque formation and rupture. An increased value of Lp-PLA2 on a lab test has been linked to initial and recurrent heart attacks, stroke, cardiovascular disease, and peripheral artery disease.4,5,6 In fact, those with elevated Lp-PLA2 activity are TWICE as likely to experience a heart attack and coronary heart disease-related death at five years after Lp-PLA2value is identified as elevated.7A 2015 article in the World Journal of Cardiology had this summary about this important cardiovascular marker: “…compelling evidence indicate that high Lp-PLA2 activity levels predict an increased risk of cardiovascular events in the general population, as well as in patients with metabolic syndrome, diabetes, and coronary heart disease.”8 It’s also a good marker to assess stroke risk. For example, people that have normal systolic blood pressure (pressure inside arteries when your heart pumps out blood) but high Lp-PLA2 are twice as likely to have a stroke.9 And those who have elevated systolic blood pressure and Lp-PLA2 levels are a whopping SEVEN times more likely to suffer a stroke!10
The first thing to do to rid yourself of the cholesterol scam is to request the Lp-PLA2 test from your doctor. This should give you a sense of whether inflammation of plaque is occurring. Labs typically used by doctors around the country can test for it. I use Lp-PLA2 as a marker to assess cardiovascular risk in people with known coronary artery disease, diabetes, and high blood pressure, as well as those with a history of smoking. However, it is also a good test to run in healthy people, as it can help predict the future development of coronary artery disease and stroke.11,12If your numbers for the marker come back high, you can then take proactive steps to halt and reverse this inflammation. As you incorporate holistic methods—such as a Mediterranean diet, exercise, fish oil, omega-7 fatty acids, turmeric, or more intensive programs such as chelation therapy—you’ll find your Lp-PLA2 levels decreasing. All of these healthy regimens are a good idea anyway, even if your level of this inflammation marker is low. Incorporating them into your program will help keep it low!
1. Dr. Stephen Sinatra. The Great Cholesterol Myth. Accessed January 21, 2017 at www.drsinatra.com/the-great-cholesterol-myth
2. Sachdeva A et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J. 2009 Jan;157(1):111-117.
3. Dr. Stephen Sinatra. The Great Cholesterol Myth. Accessed January 21, 2017 at www.drsinatra.com/the-great-cholesterol-myth
4. Jenny NS, Solomon C, Cushman M, et al. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) and risk of cardiovascular disease in older adults: Results from the Cardiovascular Health Study. Atherosclerosis. 2010;209:528-532.
5. Cushman M, Judd S, Kissela B, et al. Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and coronary heart disease risk in a biracial cohort: The reasons for geographic and racial differences in stroke (REGARDS) cohort [abstract EAS-0541]. Atherosclerosis. 2015; 241: e1-e31
6. Koenig W, Twardella D, Brenner H, et al. Lipoprotein-associated phospholipase A2 predicts future cardiovascular events in patients with coronary heart disease independently of traditional risk factors, markers of inflammation, renal function, and hemodynamic stress. Arterioscler Thromb Vasc Biol. 2006;26:1586-1593.
7. Cushman M, Judd S, Kissela B, et al. Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and coronary heart disease risk in a biracial cohort: The reasons for geographic and racial differences in stroke (REGARDS) cohort [abstract EAS-0541]. Atherosclerosis. 2015; 241: e1-e31
8. Giuseppe M et al. Lipoprotein-associated phospholipase A2 prognostic role in atherosclerotic complications. World J Cardiol. 2015 Oct 26; 7(10): 609–620.
9. Ballantyne CM et al. Lipoprotein-associated phospholipase A2, high sensitivity C-reactive protein, and risk for incident ischemic stroke in middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) study. Arch Intern Med. 2005; 165: 2479-2484.
10. Gorelick PB. Lipoprotein-associated phospholipase A2 and risk of stroke. Am J Cardiol. 2008; 101 (suppl): 34F-40F
11. Ballantyne CM et al. Lipoprotein-associated phospholipase A2, high-sensitivity C-reactive protein, and risk for incident coronary heart disease in middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) study. Circulation. 2004; 109: 837-842.
12. Daniels LB et al. Lipoprotein-associated phospholipase A2 is an independent predictor of incident coronary heart disease in an apparently healthy older population: The Rancho Bernardo Study. J Am Coll Cardiol. 2008; 51: 913-919.
